Seminars in nephrology最新文献

Cardiovascular disease poses a significant threat to individuals with kidney disease, including those affected by acute kidney injury (AKI). In the short term, AKI has several physiological consequences that can impact the cardiovascular system. These include fluid and sodium overload, activation of the renin-angiotensin-aldosterone system and sympathetic nervous system, and inflammation along with metabolic complications of AKI (acidosis, electrolyte imbalance, buildup of uremic toxins). Recent studies highlight the role of AKI in elevating long-term risks of hypertension, thromboembolism, stroke, and major adverse cardiovascular events, though some of this increased risk may be due to the impact of AKI on the course of chronic kidney disease. Current management strategies involve avoiding nephrotoxic agents, optimizing hemodynamics and fluid balance, and considering renin-angiotensin-aldosterone system inhibition or sodium-glucose cotransporter 2 inhibitors. However, future research is imperative to advance preventive and therapeutic strategies for cardiovascular complications in AKI. This review explores the existing knowledge on the cardiovascular consequences of AKI, delving into epidemiology, pathophysiology, and treatment of various cardiovascular complications following AKI.

Despite being the world's top risk factor for death and disability, hypertension awareness and control within the chronic kidney disease (CKD) population have decreased. This is particularly important considering the heightened severity and management challenges of hypertension in CKD patients, whose outcomes are often worse compared with persons with normal kidney function. Therefore, finding novel therapeutics to improve blood pressure control within this vulnerable group is paramount. Although medications that target the renin-angiotensin-aldosterone system remain a mainstay for blood pressure control in most stages of CKD, we discuss novel approaches that may expand their use in advanced CKD. We also review newer tools for blood pressure management that have emerged in recent years, including aldosterone synthase inhibitors, endothelin receptor antagonists, and renal denervation. Overall, the future of hypertension management in CKD appears brighter, with a growing arsenal of tools and a deeper understanding of this complex disease.

Atrial fibrillation (AF) is highly prevalent in patients with chronic kidney disease (CKD). It is associated with an increased risk of stroke, which increases as kidney function declines. In the general population and in those with a moderate degree of CKD (creatinine clearance 30-50 mL/min), the use of oral anticoagulation to decrease the risk of stroke has been the standard of care based on a favorable risk–benefit profile that had been established in seminal randomized controlled trials. However, evidence regarding the use of oral anticoagulants for stroke prevention is less clear in patients with severe CKD (creatinine clearance <30 mL/min) and those receiving maintenance dialysis, as these individuals were excluded from such large randomized controlled trials. Nevertheless, the direct oral anticoagulants have invariably usurped vitamin K antagonists as the preferred choice for oral anticoagulation among patients with AF across all strata of CKD based on their well-defined safety and efficacy and multiple pharmacokinetic benefits (e.g., less drug–drug interactions). This review summarizes the current literature on the role of oral anticoagulation in the management of AF among patients with CKD and highlights current deficiencies in the evidence base and how to overcome them.

A growing variety of cardiac devices are available to monitor or support cardiovascular function. The entwined nature of cardiovascular disease and kidney disease makes the relationship of these devices with kidney disease a multifaceted question relating to the use of these devices in individuals with kidney disease and to the effects of the devices and device placement on kidney health. Cardiac devices can be categorized broadly into cardiac implantable electronic devices, structural devices, and circulatory assist devices. Cardiac implantable electronic devices include devices for monitoring and managing cardiac electrical activity and devices for monitoring hemodynamics. Structural devices modify cardiac structure and include valve prostheses, valve repair clips, devices for treating atrial septal abnormalities, left atrial appendage closure devices, and interatrial shunt devices. Circulatory assist devices support the failing heart or support cardiac function during high-risk cardiac procedures. Evidence for the use of these devices in individuals with kidney disease, effects of the devices on kidney health and function, specific considerations with devices in kidney disease, and important knowledge gaps are surveyed in this article. With the growing prevalence of combined cardiorenal disease and the increasing variety of cardiac devices, kidney disease considerations are an important aspect of device therapy.

Congestion is the primary driver of hospital admissions in patients with heart failure and the key determinant of their outcome. Although intravenous loop diuretics remain the predominant agents used in the setting of acute heart failure, the therapeutic response is known to be variable, with a significant subset of patients discharged from the hospital with residual hypervolemia. In this context, urinary sodium excretion has gained attention both as a marker of response to loop diuretics and as a marker of prognosis that may be a useful clinical tool to guide therapy. Several decongestive strategies have been explored to improve diuretic responsiveness and removal of excess fluid. Sequential nephron blockade through combination diuretic therapy is one of the most used methods to enhance natriuresis and counter diuretic resistance. In this article, I provide an overview of the contemporary decongestive approaches and discuss the clinical data on the use of add-on diuretic therapy. I also discuss mechanical removal of excess fluid through extracorporeal ultrafiltration with a brief review of the results of landmark studies. Finally, I provide a short overview of the strategies that are currently under investigation and may prove helpful in this setting.

Chronic kidney disease (CKD) is highly prevalent, estimated to affect over 800 million people worldwide. Diabetes is a leading cause of kidney disease. Both diabetes and CKD are associated with a high risk of cardiovascular disease and related morbidity and mortality. Over the last several years, there has been a shift in focus toward integrating kidney and cardiovascular care, particularly in diabetes. Sodium-glucose cotransporter 2 inhibitors, glucagon-like peptide 1 receptor agonists, and nonsteroidal mineralocorticoid receptor antagonists have rapidly become cornerstones of kidney and cardiovascular risk-focused care in diabetes and CKD. However, present-day use of these agents is low, and disparities in use by race, ethnicity, age, sex, and comorbidities are apparent. Challenges in implementation of kidney protective and cardioprotective therapies include low rates of diabetes and CKD screening, lack of provider comfort and subspecialty reliance, inconsistencies across professional society guidelines, high rates of drug discontinuation, and prohibitive costs. Effective implementation of kidney protective and cardioprotective therapies necessitates a multifaceted approach and active engagement of patients, pharmacists, primary care providers, subspecialty providers, and health care system leaders as key stakeholders. Implementation efforts should be practical and incorporate collaborative, multidisciplinary team-based approaches. Successful implementation of kidney protective and cardioprotective therapies has the potential to improve overall health outcomes and ameliorate health care disparities.

The risk of arrhythmia and its management become increasingly complex as kidney disease progresses. This presents a multifaceted clinical challenge. Our discussion addresses these specific challenges relevant to patients as their kidney disease advances. We highlight numerous opportunities for enhancing the current standard of care within this realm. Additionally, this review delves into research concerning early detection, prevention, diagnosis, and treatment of various arrhythmias spanning the spectrum of kidney disease.

Cardiorenal syndrome encompasses a dynamic interplay between cardiovascular and kidney disease, and its prevention requires careful examination of multiple predisposing underlying conditions. The unequal distribution of diabetes, heart failure, hypertension, and kidney disease requires special attention because of the influence of these conditions on cardiorenal disease. Despite growing evidence regarding the benefits of disease-modifying agents (e.g., sodium-glucose cotransporter 2 inhibitors) for cardiovascular, kidney, and metabolic (CKM) disease, significant disparities remain in access to and utilization of these essential therapeutics. Multilevel barriers impeding their use require multisector interventions that address patient, provider, and health system-tailored strategies. Burgeoning literature also describes the critical role of unequal social determinants of health, or the sociopolitical contexts in which people live and work, in cardiorenal risk factors, including heart failure, diabetes, and chronic kidney disease. This review outlines (i) inequality in the burden and treatment of hypertension, type 2 diabetes, and heart failure; (ii) disparities in the use of key disease-modifying therapies for CKM diseases; and (iii) multilevel barriers and solutions to achieve greater pharmacoequity in the use of disease-modifying therapies. In addition, this review provides summative evidence regarding the role of unequal social determinants of health in cardiorenal health disparities, further outlining potential considerations for future research and intervention. As proposed in the 2023 American Heart Association presidential advisory on CKM health, a paradigm shift will be needed to achieve cardiorenal health equity. Through a deeper understanding of CKM health and a commitment to equity in the prevention, detection, and treatment of CKM disease, we can achieve this critical goal.

Heart failure with preserved ejection fraction (HFpEF) comprises approximately one-half of all diagnoses of heart failure. There is significant overlap of this clinical syndrome with chronic kidney disease (CKD), with many shared comorbid conditions. The presence of CKD in patients with HFpEF is one of the most powerful risk factors for adverse clinical outcomes, including death and heart failure hospitalization. The pathophysiology linking HFpEF and CKD remains unclear, but it is postulated to consist of numerous bidirectional pathways, including endothelial dysfunction, inflammation, obesity, insulin resistance, and impaired sodium handling. The diagnosis of HFpEF requires certain criteria to be satisfied, including signs and symptoms consistent with volume overload caused by structural or functional cardiac abnormalities and evidence of increased cardiac filling pressures. There are numerous overlapping metabolic clinical syndromes in patients with HFpEF and CKD that can serve as targets for intervention. With an increasing number of therapies available for HFpEF and CKD as well as for obesity and diabetes, improved recognition and diagnosis are paramount for appropriate management and improved clinical outcomes in patients with both HFpEF and CKD.